B15 Nervous Coordination And Muscles Flashcards

(53 cards)

1
Q

Describe the general general structure of a motor neurone

A

Cell body : contains organelles & high proportion of RER (rough endoplasmic reticulum)

Dendrons : branch into dendrites which carry impulses towards cell body

Axon : long, unbranched fibre carries nerve impulses away from cell body

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2
Q

Describe the additional features of a myelinated motor neurone

A

Schwann cells : wrap around axon many times

Myelin sheath : made from myelin-rich membranes of Schwann cells

Nodes of Ranvier : very short gaps between neighbouring Schwann cells where theres no myelin sheath

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3
Q

Name 3 processes Schwann cells are involved in

A

Electrical insulation

Phagocytosis

Nerve regeneration

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4
Q

How does an action potential pass along an unmyelinated neurone

A

1- stimulus leads to influx of Na+, first section of membrane depolarises

2 - local electrical currents cause Na+ voltage-gated channels further along membrane to open. Meanwhile, the section behind begins to repolarise

3 - sequential wave of depolarisation

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5
Q

Explain why myelinated axons conduct impulses faster than unmyelinated axons

A

Saltatory condition: impulse ‘jumps’ from one node of ranvier to another. Depolarisation cannot occur when myelin sheath acts as electrical insulator

So impulse doesn’t travel along whole axon length

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6
Q

What is resting potential

A

Potential difference (voltage) across neurons membrane when not stimulated (-50 to -90 mV, usually about -70 mV in humans).

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7
Q

How’s resting potential established

A

Membrane is more permeable to K+ than Na+

Sodium-potassium pump actively transports 3Na+ out of cell & 2K+ into cell

Establishes electrochemical gradient: cell contents more negative than extracellular environment

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8
Q

Name the stages in generating an action potential

A

Depolarisation

Repolarisation

Hyper polarisation

Return to resting potential

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9
Q

How might drugs decrease synaptic transmission

A

Inhibit release of neurotransmitter

Decrease permeability of postsynaptic membrane to ions

Hyper polarise postsynaptic membrane

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10
Q

What happens during depolarisation

A
  1. Stimulus —> facilitated diffusion of Na+ into cell down electrochemical gradient
  2. P.d. Across membrane becomes more positive
  3. If membrane reaches threshold potential (-50mV) voltage-gated Na+ channels open
  4. Significant influx of Na+ reverses p.d. to +40mV
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11
Q

What happens during repolarisation

A
  1. Voltage-gated Na+ channels close and voltage-gated K+ channels open
  2. Facilitated diffusion of K+ out of cell down their electrochemical gradient
  3. P.d. Across membrane becomes more negative
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12
Q

What happens during hyper polarisation

A
  1. ‘Overshoot’ when K+ diffuse out = p.d. Becomes more negative than resting potential
  2. Refractory period: no stimulus is large enough to raise membrane potential to threshold
  3. Voltage-gated K+ channels close & sodium-potassium pump re-establishes resting potential
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13
Q

Explain the importance of the refractory period

A

No action potential can be generated in hyperpolarised sections of membrane:
- ensures unidirectional impulse
- ensures discrete impulses
- limits frequency of impulse transmission

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14
Q

What is the ‘all or nothing’ principle

A

Any stimulus that causes the membrane to reach threshold potential will generate an action potential

All action potentials have same magnitude

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15
Q

Name the factors that affect the speed of conductance

A
  • myelin sheath
  • axon diameter
  • temperature
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16
Q

How does axon diameter affect the speed of conductance

A

Greater diameter = faster

  • less resistance to flow of ions (depolarisation & repolarisation)
  • less ‘leakage’ of ions (easier to maintain membrane potential)
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16
Q

How does temperature affect speed of conductance

A

Higher temp = faster

  • faster rate of diffusion (depolarisation & repolarisation)
  • faster respiration rate (enzyme-controlled) = more ATP for active transport to re-establish resting potential

Temp too high = membrane proteins denature

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17
Q

Suggest an appropriate statistical test to determine whether a factor has a significant effect on the speed of conductance

A

Students t-test (comparing means of continuous data)

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18
Q

Suggest appropriate units for the maximum frequency of impulse conduction

A

Hz

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19
Q

How can an organism detect the strength of a stimulus

A

Larger stimulus raises membrane to threshold potential more quickly after hyperpolarisation = greater frequency of impulses

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20
Q

What’s the function of synapses

A
  • electrical impulses cannot travel over junction between neurones
  • neurotransmitters send impulses between neurons/from neurons to effectors
  • new impulses can be initiated in several different neurons fro multiple simultaneous responses
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21
Q

Describe the structure of a synapses

A

Presynaptic neuron ends in synaptic knob:
contains lots of mitochondria, endoplasmic reticulum & vesicles of neurotransmitter

Synaptic cleft:
20-30nm gap between neurons

Postsynaptic neuron:
Has complementary receptors to neurotransmitter (ligand-gated Na+ channels)

22
Q

Outline what happens in the presynaptic cleft neuron when an action potential is transmitted from 1 neuron to another

A
  1. Wave of depolarisation travels down presynaptic neuron, causing voltage-gated Ca2+ channels to open
  2. Vesicles move towards & fuse with presynaptic membrane
  3. Exocytosis of neurotransmitter into synaptic cleft
23
Q

How do neurotransmitters cross the synaptic cleft

A

Via simple diffusion

24
Outline what happens in postsynaptic neuron when an action potential is transmitted from 1 neuron to another
1. Neurotransmitter binds to specific receptor on postsynaptic membrane 2. Ligand-gated Na+ channels open 3. If influx of Na+ raises membrane to threshold potential, action potential is generated
25
Explain why synaptic transmission is unidirectional
Only presynaptic neuron contains vesicles of neurotransmitter & only postsynaptic membrane has complementary receptors So impulse always travels presynaptic —> postsynaptic
26
Define summation and name 2 types
Neurotransmitter from several sub-threshold impulses accumulates to generate action potential: - temporal summation - spatial summation NB no summation at neuromuscular junctions
27
What’s the difference between temporal & spatial summation
Temporal = 1 presynaptic neuron releases neurotransmitter several times in quick succession Spatial = multiple presynaptic neurons release neurotransmitter
28
What are cholinergic synapses
Use acetylcholine as primary neurotransmitter. Excitatory or inhibitory. Located at: - motor end plate (muscle contraction) - preganglionic neurons (excitation) - parasympathetic postganglionic neurons (inhibition e.g. of heart or breathing rate)
29
What happens to acetylcholine from the synaptic cleft
1. Hydrolysis into Acetyl and choline by acetylcholinesterase (AChE) 2. Acetyl & choline diffuse back into presynaptic membrane 3. ATP is used to reform acetylcholine for storage in vesicles
30
Explain the importance of AChE
- prevents overstimulation of skeletal muscle cells - enables Acetyl + choline to be recycled
31
What happens in an inhibitory synapse
1. Neurotransmitter binds to and opens Cl- channels on postsynaptic membrane & triggers K+ channels to open 2. Cl- moves in & out via facilitated diffusion 3. P.d. Becomes more negative: hyperpolarisation
32
Describe the structure of a neuromuscular junction
Synaptic cleft between a presynaptic neuron and a skeletal muscle cell
33
How might drugs increase synaptic transmission
- inhibit AChE - Mimic shape of neurotransmitter
34
How might drugs decrease synaptic transmission
- inhibit release of neurotransmitter - decrease permeability of postsynaptic membrane to ions - hyperpolarisebpostsynaptic membrane
35
Name 3 types of muscle in the body and where they are located
- Cardiac = exclusively found in heart - smooth = walls of blood vessels and intestines - skeletal = attached to incompressible skeleton by tendons
36
Why does the phrase ‘antagonistic pair of muscles’ mean
Muscles can only pull, so they work in pairs to move bones around joints pairs pull in opposite directions: agonist contracts while antagonist is relaxed
37
Describe the gross structure of skeletal muscle
Muscle cells are fused together to form bundles of parallel muscle fibres (myofibrils) Arrangement ensures there’s no point of weakness between cells Each bundle is surrounded by endomycium: loose connective tissue with many capillaries
38
Describe the microscopic structure of skeletal muscle
Myofibrils = site of contraction Sarcoplasm = shared nuclei and cytoplasm with lots of mitochondria & endoplasmic reticulum Sarcolemma = folds inwards towards sarcoplasm to form form transverse (T) tubules
39
How does each band appear under an optical microscope
I-band. = light A-band = dark
40
How’s muscle contraction stimulated
1. Neuromuscular junction: action potential = volatge-gated Ca2+ channels open 2. Vesicles move towards & fuse with presynaptic membrane. 3. Exocytosis of acetylcholine (ACh), which diffuses across synaptic cleft 4. ACh binds to receptors on Na+ channel proteins on skeletal muscle cell membrane 5. Influx of Na+ = depolarisation
41
Explain role of Ca2+ in muscle contraction
1. Action potential moves through T-tubules in the sarcoplasm = Ca2+ channels in sarcoplasmic reticulum open 2. Ca2+ binds to troponin, triggering conformational Change in tropomyosin 3. Exposes binding sites on actin filaments so actinomyosin bridges can form
42
Outline ‘sliding filament theory’
1. Myosin head with ADP attached forms cross bridge with actin 2. Power stroke: myosin head changes shape & loses ADP, pulling actin over myosin 3. ATP attaches to myosin head, causing it to detach from actin 4. ATPase hydrolyses ATP —> ADP (+Pi) so myosin head can return to original position 5. Myosin head re-attaches to actin further along filament
43
How does sliding filament action cause a myofibrils to shorten
Myosin heads flex in opposite directions = actin filaments are pulled towards each other Distance between adjacent sarcomere Z lines shortens Sliding filament action occurs up to 100 times per second in multiple sarcomeres
44
State 4 peices of evidence that support the sliding filament theory
H-zone narrows I-band narrows Z-lines get closer (sarcomere shortens) A-zone remains same width (proves that myosin filaments do not shorten)
45
What happens during muscle contraction
Ca2+ is actively transported back into endoplasmic reticulum Tropomyosin once again blocks actin binding site
46
Explain the role of phosphocreatine in muscle contraction
Phosphorylation ADP directly to ATP when oxygen for aerobic respiration is limited e.g. during vigorous exercise
47
How could a student calculate the length of 1 sarcomere
1. View thin slice of muscle under optical microscope 2. Calibrate eye piece graticule 3. Measure distance from middle of 1 light band to middle of another
48
Where are slow and fast-twitch muscle fibres found in the body
Slow-twitch = sites of sustained contraction e.g. calf muscle Fast-twitch = sites of short-term, rapid, powerful contraction e.g. biceps
49
Explain the role of fast and slow twitch muscle fibres
Slow-twitch = long-duration contraction; well adapted to aerobic respiration to prevent lactate build up Fast-twitch = powerful short-term contraction; well-adapted to anaerobic respiration
50
Explain the structure + properties of slow-twitch muscle fibres
- glycogen store : many terminal ends can be hydrolysed to release glucose for respiration - contain myoglobin : higher affinity for oxygen than haemoglobin at lower partial pressures - many mitochondria : aerobic respiration produces more ATP - surrounded by many blood vessels : high supply of oxygen & glucose
51
Explain the structure and properties of fast-twitch muscle fibres
- large store of phosphocreatine - more myosin filaments - thicker myosin filaments - high conc of enzymes involved in anaerobic respiration - extensive sarcoplasmic reticulum : rapid uptake & release of Ca2+
52
What is a motor unit
One motor neuron supplies several muscle fibres, which acts simultaneously as one functional unit